Repair ultraviolet type

Direct Repair Several types of damage are repaired without removing a base or nucleotide. The best-characterized example is direct photoreactivation of cyclobutane pyrimidine dimers, a reaction promoted by DNA photolyases. Pyrimidine dimers result from an ultraviolet light-induced reaction, and photolyases use energy derived from absorbed light to reverse the dam-... 

This example inspired searches for radiation sensitive mutants in yeast. The way was led by Nakai and Matsumoto (1967) who isolated one mutant, UV which was very sensitive to ultraviolet and a second, Xj sensitive to X-rays. They went one step further than isolation and survival curves by making the double-mutant and showing that like double mutants of recA and uvr A in E. coli it was much more sensitive to UV than either single mutant alone. This was the first demonstration of the existence of more than one type or pathway of DNA repair of UV damage in yeast, and inspired the later work of Game and Cox (1972 1973 1974), Brendel and Haynes (1973) and Louise Prakash (1993) in the genetic analysis of pathways of repair in yeast. This led to the classification of the many mutant loci into epistasis groups, which are defined as those mutants which, when combined in the same strain, are no more UV-sensitive than the most sensitive of the two when alone. 

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Finally, another potential interplay between UVR and viruses occurs when they coexist with their host in a type of mutualistic relationship, where the nucleic acid of the virus is integrated in the genome of the host and is replicated with it (lysogenic state). Ultraviolet C radiation produced by germicidal lamps (max. at 254 nm) has normally been used, among other stressors, to induce the shift from lysogenic to lytic state in a complex mechanism involving the DNA repair SOS system of the host [93]. However, natural or simulated solar UVR seems not to be very efficient in this process [94,95]. 

Nucleotide-excision repair is common for DNA lesions caused by ultraviolet or chemical means, which often lead to deformed DNA structures. Figure 10.16 demonstrates how a large section of DNA containing the lesion is removed by ABC excinuclease. DNA polymerase I and DNA ligase then work to fill in the gap. This type of repair is also the most common repair for ultraviolet damage in mammals. Defects in DNA repair mechanisms can have drastic consequences. One of the most remarkable examples is the disease xeroderma pigmentosum. Affected individuals develop numerous skin cancers at an early age because... 

The polAl mutants are extraordinarily sensitive to ultraviolet irradiation because they are deficient in the 5 —> 3 exonuclease activity of DNA polymerase I and are therefore impaired in DNA repair. They have only 1% of the activity of their wild-type counterpart and cannot efficiently remove thymine dimers formed by UV light. They can, however, replicate their DNA at normal rates because DNA polymerase III is the enzyme that is primarily responsible for DNA replication. An enzyme, RNaseH, which hydrolyzes RNA only when it is base paired to DNA, likely replaces the 5 —> 3 exonuclease in processing the Okazaki fragments. 

The most well-known form of ultraviolet light—induced base damage is the pyrimidine dimer. Although the hallmark repair system for this type of... 

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